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Cheng R, Azarbal A, Currier J, et al. Tricuspid Regurgitation, the Forgotten Valvular Lesion-A Contemporary Review of Etiology, Prevalence, and Management Options. Rev Cardiovasc Med. 2015;16(3):171-81
Cheng, R., Azarbal, A., Currier, J., Thomson, L. E., Hamilton, M. A., Esmailian, F., & Azarbal, B. (2015). Tricuspid Regurgitation, the Forgotten Valvular Lesion-A Contemporary Review of Etiology, Prevalence, and Management Options. Reviews in cardiovascular medicine, 16(3), 171-81.
Cheng, Richard, et al. "Tricuspid Regurgitation, the Forgotten Valvular Lesion-A Contemporary Review of Etiology, Prevalence, and Management Options." Reviews in cardiovascular medicine vol. 16,3 (2015): 171-81.
Cheng R, Azarbal A, Currier J, Thomson LE, Hamilton MA, Esmailian F, Azarbal B. Tricuspid Regurgitation, the Forgotten Valvular Lesion-A Contemporary Review of Etiology, Prevalence, and Management Options. Rev Cardiovasc Med. 2015;16(3):171-81. PMID: 26451764.
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Rev Cardiovasc Med. 2015;16(3):171-81.

Tricuspid Regurgitation, the Forgotten Valvular Lesion-A Contemporary Review of Etiology, Prevalence, and Management Options.

Reviews in cardiovascular medicine

Richard Cheng, Amir Azarbal, Jesse Currier, Louise E J Thomson, Michele A Hamilton, Fardad Esmailian, Babak Azarbal

Affiliations

  1. Cedars-Sinai Heart Institute, Los Angeles, CA; Department of Medicine, University of Alabama Medical Center, Huntsville, AL; Division of Cardiology, VA Greater Los Angeles Healthcare System, Los Angeles, CA.

PMID: 26451764

Abstract

Tricuspid regurgitation (TR) is a common finding. Pathologic TR is an independent risk factor for mortality. TR can be classified by etiology into functional versus organic. Organic TR is caused by structural damage to the tricuspid valve (TV) by a spectrum of etiologies, including pacemaker leads and right heart biopsies, whereas functional TR is predominantly due to elevated pulmonary pressures. Atrial fibrillation and chamber enlargement, among other risk factors, are strong predictors of functional TR. Correction of elevated pulmonary pressures improves TR, and concurrent repair of severe TR at the time of left heart valve surgery improves postoperative heart failure symptoms but does not improve survival. TR repair is associated with less operative and long-term mortality than TV replacement, and demonstrates similar improvements in heart failure symptoms. Substantial residual TR remains after repair, and reoperative mortality for residual TR is considerable. Percutaneous TV replacement may offer a rescue strategy.

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